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For further information, see CMDT Part 24-17: Stupor & Coma

Key Features

Essentials of Diagnosis

  • Level of consciousness is depressed

  • Stuporous patients respond only to repeated vigorous stimuli

  • Comatose patients are unarousable and unresponsive

General Considerations

  • Coma is a major complication of serious CNS disorders

  • Coma can result from seizures, hypothermia, metabolic disturbances, meningoencephalitis, or structural lesions causing bilateral cerebral hemispheric dysfunction or a disturbance of the brainstem reticular activating system

  • A mass lesion involving one cerebral hemisphere may cause coma by compressing the brainstem

  • Abrupt onset of coma suggests

    • Subarachnoid hemorrhage

    • Brainstem stroke

    • Intracerebral hemorrhage

  • A slower onset and progression of coma occur with other structural or mass lesions

  • A metabolic cause is likely with a preceding intoxicated state or agitated delirium

Clinical Findings

Symptoms and Signs

  • In stupor, response to painful stimuli

    • Purposeful limb withdrawal from painful stimuli implies that sensory pathways from and motor pathways to the stimulated limb are functionally intact

    • Unilateral absence of responses to stimuli to both sides of the body implies a corticospinal lesion

    • Bilateral absence of responses suggests

      • Brainstem involvement

      • Bilateral pyramidal tract lesions

      • Psychogenic unresponsiveness

    • Decorticate (flexor) posturing may occur with lesions of the internal capsule and rostral cerebral peduncle

    • Decerebrate (extensor) posturing may occur

      • With dysfunction or destruction of the midbrain and rostral pons

      • In the arms accompanied by flaccidity or slight flexor responses in the legs in patients with extensive brainstem damage extending down to the pons at the trigeminal level

  • Pupils

    • Hypothalamic disease processes may lead to unilateral Horner syndrome

    • Bilateral diencephalic involvement or destructive pontine lesions lead to small but reactive pupils

    • Ipsilateral pupillary dilation with no response to light occurs with compression of the third cranial nerve, eg, with uncal herniation

    • Pupils are slightly smaller than normal but responsive to light in many metabolic encephalopathies

    • Pupils may be fixed and dilated following overdosage with atropine or scopolamine

    • Pupils may be pinpoint (but responsive) with opioids

  • Eye movements

    • Touching the cornea with a wisp of sterile gauze or cotton should elicit a blink reflex

      • A unilateral absent corneal reflex implies damage to the ipsilateral pons or a trigeminal deficit

      • Bilateral loss can be seen with large pontine lesions or in deep pharmacologic coma

    • Conjugate deviation to the side suggests

      • The presence of an ipsilateral hemispheric lesion or a contralateral pontine lesion

      • Ongoing seizures from the contralateral hemisphere

    • A mesencephalic lesion leads to downward conjugate deviation

    • Dysconjugate ocular deviation in coma implies a structural brainstem lesion (or preexisting strabismus)

  • Oculomotor responses to passive head turning

    • In response to brisk rotation, flexion, and extension of the head, conscious patients with open eyes do not exhibit contraversive conjugate eye deviation (oculocephalic reflex) unless there is voluntary visual fixation or bilateral frontal pathology

    • With cortical depression in lightly comatose patients, a brisk oculocephalic reflex ...

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